Signalling molecules in MEFs/FL
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE5402 | GEO | 2006/07/27
SECONDARY ACCESSION(S): PRJNA96215
REPOSITORIES: GEO
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Project description:In silico analysis identified signalling molecules related to Wnt (Wnt1, 2, 5a, 5b, 6, 11, 14, Wisp1, 2, sFRP1 and 2, Dkks 2 and 3) and BMP (BMP1, 4, 5) pathways. Many of these tags matched multiple transcripts in GenBank, while other potential molecules could not be detected because the transcripts either lacked an anchoring enzyme site or the site was immediately adjacent to the polyA+ sequence. Keywords: SAGE To identify potential signalling molecules (secreted or cell-cell interacting) implicated in the formation of INPs, we constructed a SAGE library from MEFs
2006-07-27 | E-GEOD-5402 | biostudies-arrayexpress
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Project description:Heterotopic ossification (HO) is the formation of extra-skeletal bone in muscle and soft tissues. Better characterization of the signaling pathways predisposing to HO is critical to identifying therapies directed against this common and potentially debilitating condition. WISP-1 (WNT1-inducible-signaling pathway protein 1) is a CCN family member and is expressed in skeletal cells during bone development or repair. Here, we sought to comprehensively explore the significance of WISP-1 across mouse and human HO. Among CCN family members, local Wisp1 expression was most highly upregulated within experimental trauma-associated HO by RNA sequencing, and increased Wisp1 corresponded to gene markers of osteochondral differentiation. WISP1 immunolocalization demonstrated conserved expression in osteochondral cells across mouse and human HO, including an FOP-like model, post-traumatic model, and human examples of non-genetic HO. Transgenic Wisp1 global knockout demonstrated an increase in cartilage and bone in a trauma-induced HO model. Microarray and in vitro culture of Wisp1 null cells suggested that WISP1 functions as a negative regulator of chondrogenic differentiation, and that Wisp1 deletion results in unrestrained endochondral HO formation. siRNA mediated WISP1 knockdown in human progenitor cells confirmed this finding. Overall, these findings suggest that endogenous WISP1 has pathophysiologic relevance in trauma-induced HO and functions as a negative regulator of ectopic chondrogenesis.
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Project description:WNT-induced secreted protein 1 (WISP1/CCN4), a member of the CCN protein family, acts as a downstream factor of the canonical WNT-signaling pathway. A dysregulated expression of WISP1 often reflects its oncogenic potential by inhibition of apoptosis, a necessary form of cell death that protect cell populations for transformation into malignant phenotypes. WISP1-signaling is also known to affect proliferation and differentiation of human mesenchymal stem cells (hMSCs), which are fundamental for the constitution and maintenance of the musculoskeletal system. Our study emphasizes the importance of WISP1-signaling for cell survival of primary human cells. Therefore, we established a successful down-regulation of endogenous WISP1 transcripts through gene silencing in hMSCs. We were able to demonstrate the consequence of cell death immediately after WISP1 down-regulation took place. Bioinformatical analyses of subsequent performed microarrays from WISP1 down-regulated vs. control samples confirmed this observation. We uncovered several clusters of differential expressed genes important for cellular apoptosis induction and immuno-regulatory processes, thereby indicating TRAIL-induced and p53-mediated apoptosis as well as IFNbeta-signaling. Since all of them act as potent inhibitors for malignant cell growth, in vitro knowledge about the connection with WISP1-signaling could help to find new therapeutic approaches concerning cancerogenesis and tumor growth in musculoskeletal tissues. We established a successful down-regulation of endogenous WISP1 transcripts through gene silencing in hMSCs. Knock-down versus controls.
2014-04-30 | E-GEOD-37603 | biostudies-arrayexpress
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Project description:The huge size, the redundancy and the great repeated portion of the bread wheat genome [Triticum aestivum (L.)], placed it among the most difficult species to be sequenced and dissected at the genetic, structural and evolutionary levels. To overcome the limitations, a strategy based on the genome compartmentalization in individual chromosomes and the subsequent production of physical maps was established within the frame of the International Wheat Genome Sequence Consortium. A total of 95,812 BAC clones of short (5AS) and long (5AL) arm-specific BAC libraries, were fingerprinted and assembled into contigs by complementary analytical approaches based on FingerPrinted Contigs and Linear Topological Contig. Combined anchoring approaches based on PCR marker screening, microarray and BlastN searches, applied to interlinked genomic tools, that is genetic maps, deletion bin map, high-density neighbor map, BAC end sequences, genome zipper and chromosome survey sequences, allowed the development of a high quality physical map, with an anchored physical coverage of 75% for 5AS and 53% for 5AL, with high portions (64 and 48%, respectively) ordered along the chromosome. The gene distribution along the wheat chromosome 5A compared with the closest related genomes showed a pattern of syntenic blocks belonging to different chromosomes of Brachypodium, rice and sorghum and regions involving translocations and inversions. The physical map presented here is currently the most comprehensive map for 5A chromosome and represents an essential resource for fine genetic mapping and map-based cloning of agronomically relevant traits, and a reference for the 5A sequencing projects. 55 DNA pools of short arm of chromsome 5A and 63 DNA pools of long arm of 5A. The DNAs derive from BAC clones of the Minimal Tiling Paths produced by physical assemly of BAC fingerprints.
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Project description:WNT-induced secreted protein 1 (WISP1/CCN4), a member of the CCN protein family, acts as a downstream factor of the canonical WNT-signaling pathway. A dysregulated expression of WISP1 often reflects its oncogenic potential by inhibition of apoptosis, a necessary form of cell death that protect cell populations for transformation into malignant phenotypes. WISP1-signaling is also known to affect proliferation and differentiation of human mesenchymal stem cells (hMSCs), which are fundamental for the constitution and maintenance of the musculoskeletal system. Our study emphasizes the importance of WISP1-signaling for cell survival of primary human cells. Therefore, we established a successful down-regulation of endogenous WISP1 transcripts through gene silencing in hMSCs. We were able to demonstrate the consequence of cell death immediately after WISP1 down-regulation took place. Bioinformatical analyses of subsequent performed microarrays from WISP1 down-regulated vs. control samples confirmed this observation. We uncovered several clusters of differential expressed genes important for cellular apoptosis induction and immuno-regulatory processes, thereby indicating TRAIL-induced and p53-mediated apoptosis as well as IFNbeta-signaling. Since all of them act as potent inhibitors for malignant cell growth, in vitro knowledge about the connection with WISP1-signaling could help to find new therapeutic approaches concerning cancerogenesis and tumor growth in musculoskeletal tissues.
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